Heart failure + Hypertension Flashcards
Pathophysiology of congestive heart failure
- In a normal heart, increased ventricular filling results in increased contraction via the Frank-Starling law → increased cardiac output
- In patients with heart failure, this mechanism fails
- As the heart continues to fail → compensatory mechanisms are activated, including an increase in heart rate, catecholamine release and RAAS activation
- These mechanisms are useful in the initial period but are usually overexpressed, thus instigating a vicious cycle
- Medications such as ACE inhibitors aim to target these compensatory pathways
Common causes of congestive cardiac heart failure
- Ischaemic heart disease
- Hypertension
- Valvular disease
- Atrial fibrillation
Symptoms of left sided heart failure
- Dyspnoea: particularly exertional
- Orthopnoea and paroxysmal nocturnal dyspnoea
- Fatigue and weakness
- Cough with pink, frothy sputum
- Cardiogenic wheeze
Signs of left sided heart failure
- Tachypnoea and tachycardia
- Cool peripheries
- Peripheral or central cyanosis
- Displaced apex beat
- Stony dull percussion: if an effusion is present
- Crackles on auscultation: coarse bi-basal crackles
- Third heart sound (S3)
Symptoms of right sided heart failure
- Swelling in the legs
- Distended abdomen
- Fatigue and weakness
Signs of right sided heart failure
- Raised JVP
- Peripheral pitting oedema
- Hepatosplenomegaly
- Ascites
Which criteria is used to classify heart failure?
The New York Heart Association (NYHA) classification system
Class 1:
- no limitation of physical activity
- ordinary physical activity does not cause symptoms (fatigue, palpitation, dyspnoea)
Class 2:
- slight limitation of physical activity
- ordinary physical activity causes symptoms
Class 3:
- marked limitation of physical activity
- less than ordinary physical activity causes symptoms
Class 4:
- all physical activity causes discomfort
- symptoms at rest
Investigations for heart failure
- Bedside
- ECG: broad QRS and evidence of LVH (high amplitude)
- Bloods
- NT-proBNP:
- >400pmol/L suggests HF and requires transthoracic ECHO within 6 weeks
- >2000pmol/L requires urgent transthoracic ECHO within 2 weeks
- Acute heart failure: urgent ECHO (usually within 48 hours)
- FBC: anaemia causes high output failure
- U&Es: CKD can cause heart failure
- TFTs: hyperthyroidism can cause high output failure
- NT-proBNP:
- Imaging
- Transthoracic ECHO: assess left ventricular ejection fraction, diastolic function
- CXR: assess heart size (PA film) and evidence of pulmonary congestion
Signs of heart failure on X-ray
- A - Alveloar oedema (batwing opacities)
- B - Kerley B lines
- C - Cardiomegaly
- D - Dilated upper lobe vessels
- E - Pleural Effusion
Management of congestive heart failure
- 1st line: Beta-blocker and ACE inhibitor: start one drug at a time. Beta-blockers (e.g. bisoprolol) and ACE inhibitors (e.g. ramipril) have been shown to reduce mortality
- 2nd line: Aldosterone antagonist (e.g. spironolactone)
Congestive cardiac failure
Despite bisoprolol, ramirpil and spironolactone, the patient is breathless at rest
What is the most appropriate next step?
- Cardiac resynchronisation therapy (CRT) or implantable cardioverter-defibrillator (ICD)
- (CRT involves biventricular pacing and forces both ventricles to contract in synchrony, thereby improving cardiac output)
- (An ICD is able to perform cardioversion, defibrillation and, in some cases, pacing)
- CRT or an ICD is generally indicated in: symptomatic patients with an ECG indicating ventricular dyssynchrony (e.g. QRS >120ms) AND LVEF <35%
- Digoxin: an alternative option, particularly for patients with atrial fibrillation and heart failure due to its inotropic effects. It does not improve prognosis in patients with heart failure
- Ivabradine: an alternative option if HR >75 bpm and LVEF <35%, and the patient is already on suitable medication (e.g. bisoprolol, ramipril and spironolactone)
- Sacubitril valsartan: if LVEF <35% (will replace ACEi)
Adjunctive management of congestive heart failure
- Fluid restriction: usually limited to <1.5L/day, but varies between patients
- Loop diuretic (e.g. furosemide): confers symptomatic relief of fluid overload but no improvement in prognosis
- Annual influenza vaccine and one-off pneumococcal vaccine
Acute heart failure - key concern
Acute heart failure can cause significant pulmonary oedema and respiratory failure
Management of acute heart failure
Stabilise
- Oxygen: is SpO2 <94% or type 1 respiratory failure
- Fluid restriction: 1.5L
- IV diuretic: furosemide infusion
- Monitor daily weights and urine output
Consider
- IV nitrates: if evidence of HTN or myocardial ischaemia; reduces preload
- Inotropes (eg dobutamine): if evidence of haemodynamic instability; improves ejection fraction
- Ventilation:
- CPAP: for type 1 respiratory failure
- Mechanical ventilation if above fail
Pathophysiology of essential hypertension
Cardiac output x peripheral resistance = Mean arterial pressure
Cardiac output = Stroke volume + Heart rate
Peripheral resistance = Vascular tone (eg activation of RAAS) + Vascular structure (eg atherosclerosis)